Magnesium is nutritionally important for maintenance of vascular integrity, but is often deficient in fatty, refined modern diets (Seelig et al., Am. J. Clin. Nutr., 27:59-79, 1974). Deleterious vascular effects of magnesium deficiency include cardiac arrhythmias and hypertension (Anderson et al., Can. Med. Assoc. J., 113:199-203, 1975). Magnesium supplements have been shown to reduce such hypertension (Dyckner et al., Brit. Med. J., 286:1847-1849, 1983; Motoyama et al., Hypertension, 113:227-232, 1989; Ryan et al., Ann. Clin. Res., 16:81-88, 1984). Intravenous administration of magnesium salts in the treatment of acute myocardial infarction has been found to decrease the subsequent incidence of arrhythmias and to improve survival. Intravenous magnesium also exerts a therapeutic effect in hypertensive crises and intractable arrhythmias (Ryan et al., 1984; Iseri, Drugs, 16:81-88, 1984; Shechter et al., Arch. Intern, Med., 152:2189-2196, 1992).
Intracellular magnesium, usually in complex with ATP, is an essential cofactor, usually in a complex with ATP, for numerous enzymes including energy-dependent membrane transport proteins such as the sodium/potassium ATPase and the calcium ATPase (Altura et al., Drugs, 28(Suppl. 1):120-142, 1984. Significant intracellular magnesium deficiency impairs the activity of these transporters, resulting in decreased intracellular levels of potassium, and increased intracellular levels of sodium and calcium.
Taurine is an amino acid present in high concentrations in excitable and secretory tissue. Its role in cardiac function has received particular attention (Huxtable, Physiol. Rev., 72:101-163, 1992; Schaffer et al., Taurine in Health and Disease, pp. 171-180, 1994). Although taurine can be synthesized endogenously from the amino acid cysteine, in mammals it is derived principally from the diet and is thus considered a "conditionally essential" nutrient. Conventional diets supply 40-400 mg of taurine daily, while vegetarian diets are extremely low in this amino acid (Huxtable, 1992).
The main function of taurine in mammals appears to be the regulation of transmembrane ionic movements, especially the regulation of calcium distribution (Schaffer et al., 1994; Huxtable, 1992; Schaffer et al., Taurine: Functional Neurochemistry, Physiology and Cardiology, pp. 217-225, 1990). However, the mechanisms of this regulation are not well understood. Taurine also exerts an anti-atherogenic action in animal models of atherosclerosis or arterial calcinosis (Petty et al., Eur. J. Pharmacol., 180:119-127, 1990; Yamauchi-Takihara et al., Biochem. Biophys. Res. Commun., 140:679-683, 1986). Taurine has also been shown to moderate blood pressure increases and thus may have a clinical antihypertensive effect.
Taurine exerts a platelet stabilizing effect both in vitro and, after oral administration, ex vivo (Hayes et al., Am. J. Clin. Nutr., 49:1211-1216, 1989; Atahanov, Arzneim-Forsch/Drug Res., 42:1311-1313, 1992). Acute intravenous administration of taurine reduces the incidence of arrhythmias in animals treated with arrhythmogenic agents and multi-gram doses have been shown to be effective in the treatment of ischemic congestive heart failure (Azuma et al., Curr. Ther. Res., 34:543-557, 1983). Thus, increased taurine intake appears to be beneficial to vascular health.
To insure optimal magnesium status, magnesium supplements are frequently advisable. Magnesium supplements are especially important for diabetics, as these individuals typically display reduced intracellular, plasma and bone levels of magnesium. Magnesium oxide is commonly used as a dietary supplement, although the bioavailability of the magnesium in this salt is far from optimal. Soluble magnesium salt complexes with good nutritional availability, including citrate and glycinate, typically are low in magnesium, the majority of the complex consisting of the counteranion which has no nutritional utility. There is a need in the art for a magnesium supplement in which the magnesium is complexed with a counteranion which itself has nutritional utility and would complement the vascular-protective actions of magnesium. The present invention addresses this need.